Improvement of endoneurial lipid abnormalities in experimental diabetic neuropathy by oxygen modification

Jeffrey K. Yao, Phillip A. Low

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

Endoneurial hypoxia and a high frequency of closed capillaries have been found in chronic experimental diabetes and human diabetic sural nerve, respectively. These findings have led to the hypothesis that the pathogenesis of diabetic neuropathy is due to endoneurial hypoxia. To evaluate the role of endoneurial hypoxia in experimental diabetic neuropathy, the effects of supplementation and deprivation of oxygen on peripheral nerve lipid biosynthesis were studied in normal control and streptozotocin-induced diabetic rats. Defective lipid biosynthesis in diabetic nerve was partially prevented by oxygen supplementation. When normal rats were placed in a hypoxic chamber, lipid abnormalities similar to those observed in diabetic nerves were demonstrated in the absence of changes in nerve free sugars. These findings suggest that endoneurial hypoxia may underlie some key biochemical abnormalities encountered in experimental diabetic neuropathy.

Original languageEnglish (US)
Pages (from-to)362-365
Number of pages4
JournalBrain Research
Volume362
Issue number2
DOIs
StatePublished - Jan 8 1986

Keywords

  • endoneurial hypoxia
  • endoneurial lipid biosynthesis
  • experimental diabetic neuropathy
  • oxygen supplementation

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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